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PubMed1997

Pharmacological manipulation of human gastrointestinal blood flow.

The splanchnic circulation is one of the largest vascular regions in man. In the past, this has been difficult to study because of methodological problems. The adapting of noninvasive Doppler techniques has made it possible to develop reproducible measurements of coeliac and superior mesenteric artery blood flow, which are the main contributors to the gastrointestinal vasculature. This has resulted in the further understanding of neurogenic and humoral control of this region in a number of physiological and pathophysiological states, and has contributed towards the knowledge of its pharmacological control. These studies are of relevance to cardiovascular homeostasis and, in particular, systemic blood pressure control which depends upon various factors including responses in different vascular regions. In this review the key physiological factors which influence pharmacological studies on this circulation will be discussed. Examples will be provided, in subjects with cardiovascular and neurological disorders, of how administration of endogenous and exogenous substances, including drugs with specific pharmacological effects, alter human gastrointestinal blood flow. These will include insulin, alcohol, the somatostatin analogue octreotide, the central acting sympatholytic clonidine and the angiotensin II-converting inhibitor captopril. The relevance of these studies to subjects with postural hypotension due to sympathetic denervation and to primary hypertension, in particular, will be discussed.

Adrenergic alpha-Agonists↗
PubMed1993

Mediation of the hypotensive action of systemic clonidine in the rat by alpha 2-adrenoceptors.

1. During the past few years it has been shown that the sympatholytic effect resulting from localized microinjection of clonidine and other imidazolines into the rostral ventrolateral medulla (RVL) results from activation of 'imidazoline' receptors (I1 receptors) rather than from an alpha 2-adrenoceptor-mediated effect. 2. The relative contributions of these two receptor systems to the hypotensive action of systemically administered clonidine have not been studied. Clonidine has affinity for both I1 and alpha 2-adrenoceptors; guanabenz represents a useful pharmacological tool, since it activates only the alpha 2-adrenoceptor. 3. Antagonists acting at both I1 and alpha 2-adrenoceptors (idazoxan) and at only alpha 2-adrenoceptors (SK&F 86466; 6-chloro-3-methyl-2,3,4,5-tetrahydro-3-benzazepine) are available. Idazoxan (1 mg kg-1, i.v.) and SK&F 86466 (3 mg kg-1, i.v.) produced an equivalent degree of blockade of the pressor response to guanabenz or clonidine in the pithed rat, a response mediated by the alpha 2-adrenoceptor. 4. Guanabenz (30 micrograms kg-1, i.v.) and clonidine (10 micrograms kg-1, i.v.) lowered blood pressure in the chloralose-anaesthetized spontaneously hypertensive rat by 48 +/- 4.6 mmHg and 44 +/- 5.4 mmHg, respectively; this response, for either agonist, was blocked by both idazoxan and SK&F 86466. 5. These data show that the hypotensive effect of intravenously administered clonidine results from activation of central alpha 2-adrenoceptors, with no significant contribution from an I1-mediated effect. Thus clonidine can lower blood pressure by different receptor mechanisms, dependent on the route of administration.

Animals↗
PubMed1996

The inhibition of antigen-induced eosinophilia and bronchoconstriction by CDP840, a novel stereo-selective inhibitor of phosphodiesterase type 4.

1. The novel tri-aryl ethane CDP840, is a potent and selective inhibitor of cyclic AMP phosphodiesterase type 4 (PDE 4) extracted from tissues or recombinant PDE 4 isoforms expressed in yeast (IC50S: 4-45 nM). CDP840 is stereo-selective since its S enantiomer (CT 1731) is 10-50 times less active against all forms of PDE 4 tested while both enantiomers are inactive (IC50S: > 100 microM) against PDE types 1, 2, 3 and 5. 2. Oral administration of CDP840 caused a dose-dependent reduction of interleukin-5 (IL-5)-induced pleural eosinophilia in rats (ED50 = 0.03 mg kg-1). The eosinophils in pleural exudates from CDP840-treated animals contained higher levels of eosinophil peroxidase (EPO) than cells from control animals, suggesting a stabilizing effect on eosinophil degranulation. CDP840 was approximately equi-active with the steroid dexamethasone in this model and was 10-100 times more potent than the known PDE 4-selective inhibitors rolipram and RP73401. The activity of CDP840 was not influenced by adrenalectomy, beta-sympathomimetics or beta-sympatholytics. 3. Antigen-induced pulmonary eosinophilia in sensitized guinea-pigs was reduced dose-dependently by CDP840 (0.01-1 mg kg-1, i.p.) and intracellular EPO levels were significantly higher. CDP840 was more potent in these activities than CT1731 or rolipram and comparable in potency to RP73401. 4. Rolipram or CDP840 were less active than dexamethasone in preventing neutrophil accumulation, or exudate formation in carrageenan-induced pleurisy in rats and thus do not exhibit general anti-inflammatory activity. 5. In sensitized guinea-pigs, aerosols of the antigen ovalbumin caused a dose-dependent bronchoconstriction demonstrated by an increase in pulmonary inflation pressure. Administration of CDP840 (0.001-1.0 mg kg-1, i.p.), 1 h before antigen challenge, resulted in dose-dependent reduction in response to antigen. This activity was not due to bronchodilatation since higher doses of CDP840 (3 mg kg-1) did not significantly change the bronchoconstrictor response to histamine. Rolipram was approximately 10 times less active than CDP840 in preventing antigen-induced bronchoconstriction. 6. These results confirm the observations that selective PDE 4 inhibitors reduce antigen-induced bronchoconstriction and pulmonary eosinophilic inflammation. CDP840 is more potent than rolipram in inhibiting native or recombinant PDE 4. Unlike the recently described potent PDE 4 inhibitor RP73401, CDP840 is more active than rolipram in the rat IL-5 model following oral administration. The novel series of tri-aryl ethanes, of which CDP840 is the lead compound, could be the basis of an orally active prophylactic treatment for human asthma.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

The role of norepinephrine in exercise impairment in congestive heart failure.

Congestive heart failure is a disorder that includes a multitude of neurohormonal responses that become maladaptive over time. Chronic sympathetic stimulation adversely affects the well-being and survival of heart failure patients and contributes to the exercise intolerance frequently seen in these patients. Norepinephrine levels have been correlated with poorer survival in heart failure patients. Administration of norepinephrine has been shown to impair exercise responses in those with congestive heart failure, and the recent effort to incorporate beta blocker therapy into the standard management of heart failure patients addresses this abnormal neurohormonal process. Studies with central-acting sympatholytics have shown mixed results. The use of drugs such as clonidine has been suggested as potentially useful therapy in the long-term management of patients with heart failure, but definitive conclusions await further study. Regular exercise has been shown to reduce resting norepinephrine levels in heart failure subjects. This may serve as an additional rationale to recommend chronic exercise for these patients.

Blood Flow Velocity↗
PubMed2004

A management of early CRPS I caused by ankle sprain: a case report.

We present a case of a 13-year-old boy who developed signs and symptoms of neuropathic pain/early Complex Regional Pain Syndrome (CRPS) Type I, formerly known as Reflex Sympathetic Dystrophy (RSD), after spraining his ankle while wrestling. Aggressive pain control, using medications and sympatholytic blocks, with physical therapy and rehabilitation, led to the resolution of his painful condition. This prevented the disease from possibly progressing to a full-blown case of CRPS I (RSD) that is very challenging to treat.

Journal Article↗
PubMed1988

Complete atrioventricular block induced by methyldopa.

We present two patients who developed complete heart block due to treatment with methyldopa. After discontinuing methyldopa, conduction disturbances completely disappeared and recurred upon rechallenge with the medication. It is assumed that methyldopa can impair the myocardial conduction system by its central sympatholytic effect. Conduction anomalies should be excluded prior to treatment with methyldopa, and during treatment with the medication, the patients should be routinely screened for the presence of conduction anomalies.

Aged↗
PubMed1994

High beta-adrenoceptor density on peripheral blood mononuclear cells in progressive multiple sclerosis: a manifestation of autonomic dysfunction?

In multiple sclerosis (MS) up-regulation of beta-adrenoceptors on peripheral blood mononuclear cells (PBMCs) has been attributed to either autonomic dysfunction, inflammation or a combination of the two. We have compared secondary progressive MS patients with normal subjects (NS) and two models of autonomic dysfunction; pure autonomic failure (PAF) and multiple system atrophy (MSA, Shy-Drager syndrome). There was up-regulation of beta-adrenoceptors on PBMCs in MS and PAF patients but not in MSA patients. Only in PAF patients beta-adrenoceptor up-regulation was correlated with low plasma levels of noradrenaline (NA) and adrenaline (Ad). In addition to studies in the basal state, measurements also were made after the centrally acting sympatholytic agent clonidine. These were combined with haemodynamic and neurohormonal measurements. After clonidine, there was a fall in blood pressure in NS and MSA patients but not in MS and PAF patients; a rise in growth hormone (GH) in NS and PAF patients but not in MS and MSA patients; and an up-regulation in PBMCs beta-adrenoceptors in NS but not in MS, MSA and PAF patients. Up-regulation of beta-adrenoceptors on PBMCs in MS could be attributed to autonomic dysfunction but the disparity between MS and PAF patients when considering their plasma levels of NA and Ad argue against. Although the neurohormonal responses to clonidine and the physiological assessment of autonomic function in progressive MS patients, demonstrate central autonomic dysfunction resembling that of the MSA patients, the normal basal beta-adrenoceptor densities in the latter, suggests that the up-regulation of these receptors is independent of the central autonomic dysfunction in MS.

Adult↗
PubMed1978

Suppresion of autonomic postganglionic discharges by pentobarbital in dogs, with or without endotoxemia.

Initial effects of pentobarbital (8 mg/kg) on autonomic efferent and afferent discharge rates were studied in 26 dogs under morphine-chloralose anesthesia. Half of the dogs were given endotoxin E. coli (1 mg/kg) before pentobarbital. The postganglionic cervical vagal efferentation of all the dogs decreased as did the postganglionic cardiac sympathetic efferentation. The heart rate of the dogs given endotoxin decreased, while an increase in heart rate with abolition of respiratory arrhythmia, was observed in dogs without endotoxin. The aortic pressure of the former dogs dropped while it fell only slightly in the latter ones. The aortic arch baroreceptor activity decreased while the changes of left atrial B-type receptor activity were not significant. The changes of the left atrial and central venous pressures were slight but those of the pulmonary arterial pressure generally paralleled the changes in the aortic pressure. Pentobarbital, accordingly, seems to exert both sympatholytic and vagolytic effects. These explain the heart rate changes, as well as the impaired cardiac contractility it evokes. The obvious impairment of cardiovascular control mechanisms by pentobarbital should be seriously considered in investigations into the cardiovascular control.

Action Potentials↗
PubMed1987

Interaction of noradrenaline, NPY and VIP with the neurogenic cholinergic response of the rat uterine cervix in vitro.

Quantitative pharmacological studies were performed on isolated uterine cervix which was obtained from oophorectomized and oestrogen-treated rats and therefore showed no spontaneous contractility. The concentration-response curves to ACh and carbacholine were to a varying degree depressed and right-shifted in the presence of NA, but not NPY or VIP. The electrically induced cholinergic contraction was potentiated in tissues from animals pretreated with reserpine or 6-OHDA, but only at high stimulation frequencies. Histochemically, both sympatholytics abolished NA from the cervical fibres, whereas immunoreactive NPY was still encountered. Tyramine in the organ bath reduced the contraction amplitude during electrical nerve stimulation concentration-dependently by a beta-adrenoceptor-sensitive mechanism. In the presence of neostigmine the amplitude was reduced by NA, but not by NPY or VIP, which, on the other hand, had an inhibitory effect in the absence of neostigmine. The results offer further support for the view that, although the cervical smooth muscle cells are equipped with adrenoceptors, the neurogenic motor response at low stimulation frequencies (around 3 HZ) is mainly cholinergic. It appears that neurally released NA is able to influence these muscle cells primarily at high frequencies. There is no clear-cut evidence that the inhibitory effects of neural NPY or VIP on the cervix of spayed, oestrogen-treated rats are mediated by postjunctional receptors.

Acetylcholine↗
PubMed1989

Interaction between sympathetic nerve fibres and epithelial transport in the rat jejunal mucosa in vivo.

The aim of this study was to elucidate the mechanisms behind the absorptive response to mesenteric nerve stimulation (MNS). Segments of rat jejunum were mounted with intact blood circulation in an 'in-vivo chamber', allowing parallel registration of net fluid transport rate (NFT) and electrical parameters of the tissue. All segments secreted fluid spontaneously, and the secretion rate was inversely correlated to the corresponding potential difference (PD) across the segment. The secretion was not inhibited by atropine. The nicotinic antagonist hexamethonium (Hx) inhibited the secretion and changed the relationship between PD and NFT. MNS reversed the secretion into an absorption (absorptive response) and decreased PD and short-circuit current (SCC) (electrogenic response). Total tissue resistance (Rt) was not significantly changed. The absorptive response increased at high control secretion rates and the electrogenic response increased at high control PD levels. The electrogenic response was inversely related to the absorptive response; however, the presence of Hx reversed this correlation. Guanethidine, a sympatholytic agent, eliminated all effects of MNS. Phentolamine eliminated the absorptive response but not the electrogenic response, and the remaining electrogenic response was not sensitive to propranolol (a beta-adrenergic antagonist). Hx induced similar but smaller effects than MNS, and after Hx treatment the MNS effects were reduced. We conclude: (1) Fluid secretion in our model involves a mechanism other than electrogenic Cl- secretion. (2) MNS activates sympathetic nerve fibres, which enhance fluid absorption and decrease PD and SCC. (3) The absorptive and electrogenic responses involve partly separate transport mechanisms. (4) Both responses are partly due to the inhibition of intramural secretory nervous pathways. (5) Some sympathetic nerve fibres interact directly with the epithelium.

Adrenergic Fibers↗
PubMed1999

Molecular pathology in the obese spontaneous hypertensive Koletsky rat: a model of syndrome X.

The SHROB rat is a unique strain with genetic obesity, hypertriglyceridemia, hyperinsulinemia, renal disease with proteinuria, and genetically determined hypertension, characteristics paralleling human Syndrome X. The obese phenotype results from a single homozygous recessive trait, designated faK, and is allelic with the Zucker fatty trait (fa), but of distinct origin. The faK mutation is a premature stop codon in the extracellular domain of the leptin receptor, resulting in a natural receptor knockout. The SHROB are glucose intolerant compared to heterozygous or wild-type SHR, but retain fasting euglycemia even on a high sucrose diet, suggesting that diabetes requires polygenic interaction with additional modifier genes. Insulin-stimulated phosphorylation of tyrosine residues on the insulin receptor and on the associated docking protein IRS-1 are reduced in skeletal muscle and liver compared to SHR, due mainly to diminished expression of insulin receptor and IRS-1 proteins. Despite multiple metabolic derangements and severe insulin resistance, hypertension is not exacerbated in SHROB compared to SHR. Thus, insulin resistance and hypertension are independent in this model. Increased activity of the sympathetic nervous system may be a common factor leading by separate pathways to hypertension and to insulin resistance. We studied the chronic effects of sympathetic inhibition with moxonidine on glucose metabolism in SHROB. Moxonidine (8 mg/kg/day), a selective I1-imidazoline receptor agonist, not only reduced blood pressure but also ameliorated glucose intolerance. Moxonidine reduced fasting insulin by 47% and plasma free fatty acids by 30%. Moxonidine enhanced expression and insulin-stimulated phosphorylation of IRS-1 in skeletal muscle by 74 and 27%, respectively. Thus, central sympatholytic therapy not only counters hypertension but also insulin resistance, glucose tolerance, and hyperlipidemia in the SHROB model of Syndrome X.

Animals↗
PubMed1979

Parasympathetic degeneration secretion of saliva in rats.

In rats under chloralose anaethesia saliva was found to flow from the submandibular and parotid glands previously subjected to (partial) postganglionic parasympathetic denervation. Secretion started in the submandibular glands 8.8-11.8 hours, and in the parotid glands 14.0-12.6 hours after the denervation and lasted about 7 hours in both glands. It was not abolished by sympatholytic drugs but by atropine. It is regarded as an example of the "degeneration activity" described in many organs and species and provides a method for prolonged stimulation of salivary glands in rats.

Animals↗
PubMed1967

Effects of physalaemin on some exocrine secretions of dogs and rats.

1. Physalaemin, an endecapeptide recently found in the skin of the South American amphibian Physalaemus fuscumaculatus, possesses, besides a marked hypotensive action and a powerful sialogogic activity, also a stimulant activity on other exocrine secretions.2. Exocrine structures which were more potently stimulated by the peptide were lacrimal glands and exocrine pancreas. In the anaesthetized dog the threshold lacrimatory dose was 0.05-0.3 mug/kg; in the rat the threshold dose was 2.5-5 mug/kg. The minimum active dose on exocrine pancreas of the dog was 0.05-0.5 mug/kg.3. Physalaemin did not influence the gastric acid secretion of the dog at the maximum tolerated dose (40 mug/kg). Gastric acid secretion of the rat was stimulated very little if at all.4. In the dog the peptide caused some changes in the bile flow which were connected more with contracture of the gall-bladder than with a true secretory stimulant activity. In the rat the peptide was completely ineffective.5. The results obtained after administration of sympatholytic and parasympatholytic agents suggest that the action of the peptide is at least partly independent from the autonomic nervous system.

Journal Article↗
PubMed1968

Shivering and non-shivering therogenesis during summit metabolism in young lambs.

1. Summit metabolism of lambs declined steadily from about 3.5 l. O(2)/kg.hr during the first day of life, to about 2.0 l. O(2)/kg.hr at 2 months of age.2. The contributions of shivering and non-shivering thermogenesis to these changes were estimated by three independent methods; non-shivering thermogenesis was stimulated by catecholamines in a thermoneutral environment, shivering was suppressed by curariform drugs during summit metabolism, and an attempt was made to suppress non-shivering thermogenesis during summit metabolism by use of the sympatholytic drugs phentolamine and propranolol. Drugs were given by intravenous infusion during measurement of oxygen consumption in a closed circuit respiration chamber.3. ;Resting' metabolic rate of lambs during the first day of life was increased two to three-fold, from 1 l. O(2)/kg.hr, by either adrenaline or noradrenaline infused at 1-10 mug/kg.min. The increase declined with increasing age of lamb and was virtually absent by 3 weeks. The response to catecholamines appeared maximal at the dose levels used.4. Muscular paralysis induced by suxamethonium or gallamine reduced summit metabolism by about 2 l. O(2)/kg.hr in all lambs examined within the first 2 months of life. The residual metabolic rate, and the metabolic response to catecholamines under thermoneutral conditions, declined with age in the same manner, and their magnitudes were similar.5. Summit metabolism in lambs aged up to 2 months was depressed to varying degrees by the sympathetic inhibitors phentolamine, propranolol and hexamethonium. The depression with propranolol was greater, and the decline with age clearer, than with phentolamine. Hexamethonium and phentolamine depressed blood pressure, propranolol decreased heart rate and phentolamine and propranolol each suppressed shivering in some experiments.6. In 1 day-old lambs estimates of non-shivering thermogenesis, by the various methods, ranged from 0.8 to 1.4 l. O(2)/kg.hr (mean 1.1 l. or 31% of summit metabolism), and the estimates of shivering ranged from 1.3 to 1.9 l. O(2)/kg.hr (mean 1.6 l. or 46% of summit metabolism). However, in lambs 1-month old, estimates of non-shivering thermogenesis from sympathetic inhibition (0.6 and 0.8 l. O(2)/kg.hr) were considerably higher than estimates from muscular paralysis or stimulation by catecholamines (0.2 and 0.1 l. O(2)/kg.hr). It is suggested that the depression of summit metabolism by the sympathetic inhibitors is not solely due to specific inhibition of non-shivering thermogenesis, at least in the older lambs.7. The possession of a non-shivering thermogenic mechanism in addition to shivering is of clear survival value to new-born lambs.

Age Factors↗
PubMed1998

Mechanism of the acute pressor effect and bradycardia elicited by diaspirin crosslinked hemoglobin in anesthetized rats.

Diaspirin crosslinked hemoglobin (DCLHb) is a chemically stabilized hemoglobin (Hb) that induces an increase in blood pressure and a decrease of heart rate when injected intravenously in some animals. The mechanism by which DCLHb elicits these hemodynamic effects was studied in pentobarbital-anesthetized, vagotomized rats using a variety of drugs known for their inhibitory action towards endogenous hemodynamically active systems. The hypertensive episode elicited by DCLHb (100 or 400 mg.kg-1) was attenuated in animals pretreated with NG-nitro-L-arginine (inhibitor of nitric oxide synthases) throughout the 30-min period of observation, but it was not reduced in those pretreated with a variety of sympatholytic drugs (e.g., prazosin), atropine, BIBP-3226 (neuropeptide Y antagonist), indomethacin, [1-(beta-mercapto-beta,beta-cyclopentanemethylene propionic acid), 2-(0-methyl) tyrosine]-Arg8 vasopressin (vasopressin antagonist), losartan (angiotensin antagonist), bosentan (endothelin antagonist), or L-arginine-(nitric oxide precursor), compared with control animals. With the exception of propranolol and BIBP-3226, none of the aforenamed inhibitors reduced the amplitude of the bradycardia associated with the pressor effect of DCLHb. These results suggest that: (i) the acute (< 30 min) pressor activity of DCLHb in our animal model requires the presence of an endogenous nitric oxide generating system to be expressed; (ii) the bradycardia elicited by DCLHb might involve the participation of neuropeptide Y and (or) its NPY-1 receptors, but it is unlikely to involve a baroreceptor-mediated vagal reflex, at least in our animal model.

Animals↗
PubMed1987

The renal afferent nerves in the pathogenesis of hypertension.

The renal nerves play a role in the pathogenesis of hypertension in a number of experimental models. In the deoxycorticosterone acetate - salt (DOCA-NaCl) hypertensive rat and the spontaneously hypertensive rat (SHR) of the Okamoto strain, total peripheral renal denervation delays the development and blunts the severity of hypertension and causes an increase in urinary sodium excretion, suggesting a renal efferent mechanism. Further, selective lesioning of the renal afferent nerves by dorsal rhizotomy reduces hypothalamic norepinephrine stores without altering the development of hypertension in the SHR, indicating that the renal afferent nerves do not play a major role in the development of hypertension in this genetic model. In contrast, the renal afferent nerves appear to be important in one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertensive rats (1K, 1C and 2K, 1C, respectively) and in dogs with chronic coarctation hypertension. Total peripheral renal denervation attenuates the severity of hypertension in these models, mainly by interrupting renal afferent nerve activity, which by a direct feedback mechanism attenuates systemic sympathetic tone, thereby lowering blood pressure. Peripheral renal denervation has a peripheral sympatholytic effect and alters the level of activation of central noradrenergic pathways but does not alter sodium or water intake or excretion, plasma renin activity or creatinine clearance, suggesting that efferent renal nerve function does not play an important role in the maintenance of this form of hypertension. Selective lesioning of the renal afferent nerves attenuates the development of hypertension, thus giving direct evidence that the renal afferent nerves participate in the pathogenesis of renovascular hypertension.

Afferent Pathways↗
PubMed2004

Pulse-synchronous sympathetic burst power as a new index of sympathoexcitation in patients with heart failure.

The upper limit of incidence of muscle sympathetic neural bursts can lead to underestimation of sympathetic activity in patients with severe heart failure. This study aimed to evaluate the pulse-synchronous burst power of muscle sympathetic nerve activity (MSNA) as a more specific indicator that could discriminate sympathetic activity in patients with heart failure. In 54 patients with heart failure, the pulse-synchronous burst power at the mean heart rate was quantified by spectral analysis of MSNA. Thirteen patients received a central sympatholytic agent (guanfacine) for 5 days to validate the feasibility of this new index. Both burst incidence and plasma norepinephrine level showed no significant difference between patients in New York Heart Association functional class III (94 +/- 6 per 100 heartbeats and 477 +/- 219 pg/ml, respectively) and class II (79 +/- 14 per 100 heartbeats and 424 +/- 268 pg/ml, respectively). In contrast, the burst power was useful for discriminating patients in class III from those in class II (61 +/- 8% vs. 39 +/- 10%; P < 0.05). Inhibition of sympathetic nerve activity by guanfacine was more sensitively reflected by the change of burst power (-36 +/- 25%) than by that of burst incidence (-12 +/- 14%; P < 0.001). The sympathetic burst power reflects both burst frequency and amplitude independently of the absolute values and provides a sensitive new index for interindividual comparisons of sympathetic activity in patients with heart failure.

Adult↗
PubMed1984

Alpha 1-adrenoceptor blockade in renal hypertensive rats with low and high renin levels.

A total of 75 male Wistar rats with one-kidney, one-clip renal hypertension was maintained on either a regular (RNa) or a low-salt (LNa) diet for 3 wk after clipping. Blood pressure in the unanesthetized rats was equally elevated independent of sodium intake. Plasma renin activity was higher in LNa animals, and blood pressure was renin dependent only in this group, as evidenced by the blood pressure response to 10 mg/kg captopril iv. There was no significant difference in plasma catecholamines between RNa and LNa rats, although in the former the sympathetic nervous system is believed to play a major role in sustaining high blood pressure. The acute intravenous administration of 0.5 mg/kg prazosin did not induce a more pronounced blood pressure fall in the RNa rats. Prazosin enhanced plasma norepinephrine levels similarly in both groups, but epinephrine levels only rose in the LNa animals. Prazosin also markedly stimulated plasma renin activity rendering blood pressure renin dependent even in RNa rats. Thus, using alpha 1-adrenoceptor blockade, it has not been possible to demonstrate that the blood pressure elevation of salt-repleted one-kidney, one-clip renal hypertensive rats is due to an enhanced sympathetic nerve activity. Data obtained with sympatholytic agents must be interpreted with great caution if renin activity cannot be kept unchanged.

Animals↗